The mitral valve is a complex structure located between the left atrium and ventricle of the mammalian heart. During systole, large pressures (e.g., greater than 120 mmHg) are imposed on the closed mitral valve. The mitral valve leaflets resist these pressures to prevent mitral regurgitation, which can cause serious cardiac complications. The mitral valve includes two leaflets (anterior and posterior) whose free edges are tethered to the wall of the left ventricle at the papillary muscles via the chordae tendinae. The basal edges of the leaflets are attached to the left ventricle via a fibrous annular ring. The anterior leaflet is a single continuous membrane, and the posterior leaflet is made up of three scallops with the central scallop being the largest.
Although there are multiple components of the mitral valve complex that can lead to dysfunction, a loss of structural integrity of the mitral valve leaflets to withstand systolic pressure can be detrimental to mitral valve performance. A specific mitral valve syndrome called mitral valve prolapse occurs when the leaflets billow back into the left atrium during systole, typically resulting in compromised mitral valve and cardiac function. Cardiologic hallmarks of mitral valve prolapse include superior displacement, such as more than 2 mm, of one or both of the leaflets into the left atrium.
Clinically, there are two distinct patient groups with mitral valve prolapse. The first group is typically younger females, and the majority of this group do not require intervention. The second group is older males with moderate to severe mitral regurgitation and thickening leaflets. Histological analysis of autopsied mitral valve prolapse leaflets from this second patient group typically reveals disrupted and/or fragmented collagen architecture with enhanced quantity of proteogylcans. This disrupted architecture is called myxomatous mitral valve disease. Because of the disrupted architecture of the myxomatous mitral valve leaflets, collagen fibers are unable to provide the neaded structural integrity to appose left ventricle pressure during systole, and the leaflet(s) displaces into the atrium, prohibiting closure and leading to mitral regurgitation.
Standard treatments for myxomatous mitral valve disease are surgical repair or replacement. Both repair and replacement of the mitral valve are expensive, potentially invasive procedures with substantial recovery times. Percutaneous edge-to-edge repair procedures can be used in some cases of myxomatous mitral valve disease, which avoids open-chest surgery and reduces hospital stay and recovery time. However, the current mode of edge-to-edge repair has a significant detractor in that it can form a double-orifice mitral valve, and the long-term fluid mechanics and left ventricle remodeling of this flow pattern are not well-understood. Moreover, if the degree of myxomatous degeneration is high, the edge-to-edge technique may not be suitable. Edge-to-edge repairs are also not suitable for many patients, including those with ischemic mitral regurgitation, recurrent mitral regurgitation after complex mitral valve repair, or mitral regurgitation associated with papillary muscle displacement. On the other hand, mitral valve replacement surgeries typically involve open-heart surgery, which can be problematic, especially in an older patient population.